CSF protein, blood brain barriers and Reiber’s hypotheses

A patient with GBS-like symptoms and elevated protein in the CSF – why is the protein high? What do you need to distinguish between local inflammation, reduced blood-csf-barrier-function and reduced resorption?

We follow Reiber in one of his many articles in CSF books or the lab bible (Lothar Thomas. Labor und Diagnose) and discuss the intricacies of CSF production, dynamics and resorption. To be honest, I still don’t really understand where CSF is generated, but Reiber says it’s not by filtration and gives proof for it. He also reduces most of the elevated protein to reduced CSF flow – panta rhei. It all looks quite convincing, so we test the theory against the problem of elevated protein in the one most important differential for GBS, namely cervical myelopathy due to decompensated degenerative cervical myelopathy with blocked CSF passage (“Stop-Liquor”): do you really understand why the protein is elevated in this case?

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